武汉大学人民医院急诊科 湖北 武汉 430060
任永栋,男,1999—,医学硕士生,主要从事脓毒症的基础与临床研究, E‑mail:2022283020123@whu.edu.cn
李文强,男,1967—,医学博士,主任医师,硕士生导师,主要从事脓毒症的基础与临床研究,E‑mail:wenqiangli@whu.edu.cn
收稿:2024-11-11,
纸质出版:2025-11-25
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任永栋,陈海瑞,胡念丹等.IL‑5抑制caspase‑1细胞焦亡信号通路减轻脓毒症小鼠急性肾损伤[J].武汉大学学报(医学版),2025,46(11):1388-1393.
REN Yongdong,CHEN Hairui,HU Niandan,et al.IL‑5 alleviates acute kidney injury in septic mice by inhibiting the caspase‑1 pyroptosis signaling pathway[J].Medical Journal of Wuhan University,2025,46(11):1388-1393.
任永栋,陈海瑞,胡念丹等.IL‑5抑制caspase‑1细胞焦亡信号通路减轻脓毒症小鼠急性肾损伤[J].武汉大学学报(医学版),2025,46(11):1388-1393. DOI: 10.14188/j.1671-8852.2024.0867.
REN Yongdong,CHEN Hairui,HU Niandan,et al.IL‑5 alleviates acute kidney injury in septic mice by inhibiting the caspase‑1 pyroptosis signaling pathway[J].Medical Journal of Wuhan University,2025,46(11):1388-1393. DOI: 10.14188/j.1671-8852.2024.0867.
目的
2
探究白细胞介素‑5(IL‑5)对脓毒症所致小鼠急性肾损伤的影响及机制。
方法
2
盲肠结扎穿孔法(CLP)构建小鼠脓毒症急性肾损伤模型,40只小鼠随机分为假手术(Sham)组、脓毒症模型(CLP)组、IL‑5干预(CLP+IL‑5)组、假手术+IL‑5(Sham+IL‑5)组。造模后24 h取材,ELISA检测各组小鼠血清中肿瘤坏死因子‑α(TNF‑α)、IL‑6、IL‑1β、肌酐(Scr)、尿素氮(BUN)的含量;HE染色观察肾脏病理学改变;TUNEL染色检测肾组织细胞凋亡情况;Western Blot检测肾脏组织中NLRP3、caspase‑1蛋白表达。
结果
2
IL‑5减轻了脓毒症小鼠肾脏病理损伤程度,降低脓毒症小鼠血清中TNF‑α、IL‑6、IL‑1β、Scr、BUN的浓度及肾组织NLRP3、caspase‑1蛋白表达水平(
P
<
0.05),抑制细胞凋亡与炎症反应,改善脓毒症相关急性肾损伤。
结论
2
IL‑5能够抑制全身炎症反应,从而减轻脓毒症所致的急性肾损伤,其作用机制可能与IL‑5抑制NLRP3炎症小体的激活以及caspase‑1介导的经典细胞焦亡途径的活化相关。
Objective
2
To explore the effects of interleukin⁃5 (IL⁃5) on sepsis⁃induced acute kidney injury in mice.
Methods
2
A mouse model of septic acute kidney injury was established using the cecal ligation and puncture (CLP) method. Forty mice were randomly assigned to four groups: Sham group
sepsis model (CLP) group
IL‑5 intervention (CLP+IL‑5) group
and Sham+IL‑5 group. Tissue samples were collected 24 hours post‑modeling. ELISA was utilized to measure serum levels of tumor necrosis factor‑alpha (TNF‑α)
IL‑6
IL‑1β
creatinine (Scr)
and blood urea nitrogen (BUN). HE staining was performed to evaluate renal tissue pathology
TUNEL staining to assess apoptosis
and Western Blot to determine NLRP3 and caspase‑1 proteins expression in kidney tissues.
Results
2
IL‑5 significantly attenuated renal histological injury in septic mice. It reduced serum levels of TNF‑α
IL‑6
IL‑1β
Scr
and BUN
and suppressed NLRP3 and caspase‑1 protein expression in kidney tissues (
P
<
0.05). By inhibiting apoptosis and the inflammatory response
IL‑5 markedly ameliorated sepsis⁃associated acute kidney injury.
Conclusion
2
IL‑5 inhibits the systemic inflammatory response
thereby mitigating acute kidney injury induced by sepsis. This protective effect may be mediated through the suppression of NLRP3 inflammasome activation and inhibition of the caspase‑1‑mediated classical pyroptosis pathway.
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